Bronchoalveolar Lavage Cytological Alveolar Damage in Patients
Bronchoalveolar Lavage Cytological Alveolar Damage in Patients
Introduction: Histological examination of lung specimens from patients with pneumonia shows the presence of desquamated pneumocytes and erythrophages. We hypothesized that these modifications should also be present in bronchoalveolar lavage fluid (BAL) from patients with hospital-acquired pneumonia.
Methods: We conducted a prospective study in mechanically ventilated patients with clinical suspicion of pneumonia. Patients were classified as having hospital-acquired pneumonia or not, in accordance with the quantitative microbiological cultures of respiratory tract specimens. A group of severe community-acquired pneumonias requiring mechanical ventilation during the same period was used for comparison. A specimen of BAL (20 ml) was taken for cytological analysis. A semiquantitative analysis of the dominant leukocyte population, the presence of erythrophages/siderophages and desquamated type II pneumocytes was performed.
Results: In patients with confirmed hospital-acquired pneumonia, we found that 13 out of 39 patients (33.3%) had erythrophages/siderophages in BAL, 18 (46.2%) had desquamated pneumocytes and 8 (20.5%) fulfilled both criteria. Among the patients with community-acquired pneumonia, 7 out of 15 (46.7%) had erythrophages/siderophages and 6 (40%) had desquamated pneumocytes on BAL cytology. Only four (26.7%) fulfilled both criteria. No patient without hospital-acquired pneumonia had erythrophages/siderophages and only 3 out of 18 (16.7%) had desquamated pneumocytes on BAL cytology.
Conclusion: Cytological analysis of BAL from patients with pneumonia (either community-acquired or hospital-acquired) shows elements of cytological alveolar damage as hemorrhage and desquamated type II pneumocytes much more frequently than in BAL from patients without pneumonia. These elements had a high specificity for an infectious cause of pulmonary infiltrates but low specificity. These lesions could serve as an adjunct to diagnosis in patients suspected of having ventilator-associated pneumonia.
Pneumonia is a common problem in critical care patients. Ventilator-associated pneumonia (VAP) complicates the course of as much as 27% of patients requiring mechanical ventilation. Because mortality in patients with pneumonia is high and clinical studies have shown that an adequate antimicrobial treatment improves outcome, it is mandatory to identify infected patients precisely and give them effective treatment.
Unfortunately, at present there are no consensus criteria for the diagnosis of VAP. Although clinical criteria (purulent tracheal secretions, fever), combined with the presence of new or worsening infiltrates on a chest radiogram or leukocytosis, are sensitive, they have poor specificity for diagnosing VAP. Using solely clinical criteria entails a high risk of dispensing unnecessary antimicrobial treatment with the risk of emergence of multidrug-resistant organisms. So far no biological test has proven useful in differentiating patients with and without pneumonia, despite very promising candidates. Most diagnostic strategies rely today on quantitative cultures of samples of bronchial secretions from distal airways such as protected specimen brush, bronchoalveolar lavage fluid (BAL) or protected telescopic catheters (PTC) performed either under fibro-bronchoscopic guidance or in a blind manner. Even though there is still controversy over whether such techniques should be used as diagnostic criteria or just for guiding antibacterial treatment after diagnosis has been made, they are extensively recommended and used in clinical practice. Contrasting with the large amount of information about the quantitative culture of bronchial specimens, little has been published on the cytological aspects of BAL in pneumonia. Previous reports emphasized the lack of specificity of neutrophil predominance. From all cytological information that can be gathered, so far only the presence of intracellular pathogens in more than 1 to 5% of BAL neutrophils has been retained as being highly suggestive of bacterial pneumonia in ventilated patients.
The lung response to local aggression after infectious pneumonia results in epithelial damage, edema, hemorrhage, the intra-alveolar accumulation of polymorphonuclear neutrophils and hyaline membrane formation. Macrophages that engulf red blood cells take the aspect of erythrophagocytes and later siderophages. The presence of one of these elements can be a useful marker of active alveolar hemorrhage. Furthermore, damage at the epithelial alveolar level can lead to desquamation of dystrophic pneumocytes. These cells can eventually be found in BAL, as shown in some patients with acute lung injury. Jacobs et al.. have described the presence of desquamated type II pneumocytes in the BAL from patients with various types of pulmonary infection. Thus, the presence of lesions of alveolar damage associated with alveolar hemorrhage and desquamated type II pneumocytes in BAL could help to differentiate pneumonia from other causes of pulmonary infiltrates (such as atelectasis or pulmonary edema) and could be of diagnostic importance.
The aim of our study was to evaluate the incidence of these findings in patients with severe pneumonia who were receiving mechanical ventilation.
Introduction: Histological examination of lung specimens from patients with pneumonia shows the presence of desquamated pneumocytes and erythrophages. We hypothesized that these modifications should also be present in bronchoalveolar lavage fluid (BAL) from patients with hospital-acquired pneumonia.
Methods: We conducted a prospective study in mechanically ventilated patients with clinical suspicion of pneumonia. Patients were classified as having hospital-acquired pneumonia or not, in accordance with the quantitative microbiological cultures of respiratory tract specimens. A group of severe community-acquired pneumonias requiring mechanical ventilation during the same period was used for comparison. A specimen of BAL (20 ml) was taken for cytological analysis. A semiquantitative analysis of the dominant leukocyte population, the presence of erythrophages/siderophages and desquamated type II pneumocytes was performed.
Results: In patients with confirmed hospital-acquired pneumonia, we found that 13 out of 39 patients (33.3%) had erythrophages/siderophages in BAL, 18 (46.2%) had desquamated pneumocytes and 8 (20.5%) fulfilled both criteria. Among the patients with community-acquired pneumonia, 7 out of 15 (46.7%) had erythrophages/siderophages and 6 (40%) had desquamated pneumocytes on BAL cytology. Only four (26.7%) fulfilled both criteria. No patient without hospital-acquired pneumonia had erythrophages/siderophages and only 3 out of 18 (16.7%) had desquamated pneumocytes on BAL cytology.
Conclusion: Cytological analysis of BAL from patients with pneumonia (either community-acquired or hospital-acquired) shows elements of cytological alveolar damage as hemorrhage and desquamated type II pneumocytes much more frequently than in BAL from patients without pneumonia. These elements had a high specificity for an infectious cause of pulmonary infiltrates but low specificity. These lesions could serve as an adjunct to diagnosis in patients suspected of having ventilator-associated pneumonia.
Pneumonia is a common problem in critical care patients. Ventilator-associated pneumonia (VAP) complicates the course of as much as 27% of patients requiring mechanical ventilation. Because mortality in patients with pneumonia is high and clinical studies have shown that an adequate antimicrobial treatment improves outcome, it is mandatory to identify infected patients precisely and give them effective treatment.
Unfortunately, at present there are no consensus criteria for the diagnosis of VAP. Although clinical criteria (purulent tracheal secretions, fever), combined with the presence of new or worsening infiltrates on a chest radiogram or leukocytosis, are sensitive, they have poor specificity for diagnosing VAP. Using solely clinical criteria entails a high risk of dispensing unnecessary antimicrobial treatment with the risk of emergence of multidrug-resistant organisms. So far no biological test has proven useful in differentiating patients with and without pneumonia, despite very promising candidates. Most diagnostic strategies rely today on quantitative cultures of samples of bronchial secretions from distal airways such as protected specimen brush, bronchoalveolar lavage fluid (BAL) or protected telescopic catheters (PTC) performed either under fibro-bronchoscopic guidance or in a blind manner. Even though there is still controversy over whether such techniques should be used as diagnostic criteria or just for guiding antibacterial treatment after diagnosis has been made, they are extensively recommended and used in clinical practice. Contrasting with the large amount of information about the quantitative culture of bronchial specimens, little has been published on the cytological aspects of BAL in pneumonia. Previous reports emphasized the lack of specificity of neutrophil predominance. From all cytological information that can be gathered, so far only the presence of intracellular pathogens in more than 1 to 5% of BAL neutrophils has been retained as being highly suggestive of bacterial pneumonia in ventilated patients.
The lung response to local aggression after infectious pneumonia results in epithelial damage, edema, hemorrhage, the intra-alveolar accumulation of polymorphonuclear neutrophils and hyaline membrane formation. Macrophages that engulf red blood cells take the aspect of erythrophagocytes and later siderophages. The presence of one of these elements can be a useful marker of active alveolar hemorrhage. Furthermore, damage at the epithelial alveolar level can lead to desquamation of dystrophic pneumocytes. These cells can eventually be found in BAL, as shown in some patients with acute lung injury. Jacobs et al.. have described the presence of desquamated type II pneumocytes in the BAL from patients with various types of pulmonary infection. Thus, the presence of lesions of alveolar damage associated with alveolar hemorrhage and desquamated type II pneumocytes in BAL could help to differentiate pneumonia from other causes of pulmonary infiltrates (such as atelectasis or pulmonary edema) and could be of diagnostic importance.
The aim of our study was to evaluate the incidence of these findings in patients with severe pneumonia who were receiving mechanical ventilation.
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